Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007879
Markus Rottmann, A. Kleber, M. Barkagan, J. Sroubek, E. Leshem, Ayelet Shapira-Daniels, A. Buxton, E. Anter
BACKGROUND In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit. METHODS In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit. RESULTS Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT. CONCLUSIONS Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.
背景:在梗死相关性室性心动过速(VT)中，该电路通常对应于窦性心律(SR)期间激活减慢的位置。然而，SR期间的激活减慢与再入脆弱性之间的关系以及与VT电路组成的相关性尚不清楚。这项研究考察了SR期间的激活减慢和再入脆弱性之间的关系，并将这些区域与回路的组成部分联系起来。方法在猪梗死愈合模型中，比较SR和VT的心内膜激活速度的空间分布。使用激活和夹带映射将峡部定义为电路内显示舒张活动的区域，而将旁观者定义为电路外显示舒张活动的区域。结果15头猪中，9头猪可诱导VT(每头5.2±3.0)，6头猪在2个传动系的4个左室和左室部位进行6次额外刺激后仍不能诱导VT。伴有VT的梗死在sr期间具有更大程度的激活减慢。诱导性和非诱导性梗死的最小心内膜激活速度切断≤0.1 m/s (P=0.015)。SR期间最大心内膜减慢的区域对应于室速峡(曲线下面积=0.84 95% CI, 0.78-0.90)，而旁观者部位在SR期间表现出接近正常的激活。室速电路复杂，41.7%表现出不连续传播，伴有缓慢传导的壁内桥和延迟的准同步心内膜激活。结论静息期心肌激活减慢可能是区分易发生室性心动过速梗死和不易发生室性心动过速梗死的重要依据。静息期心肌激活减慢的部位与形成室性心动过速的部位相对应，而与旁观者部位不一致。
{"title":"Activation During Sinus Rhythm in Ventricles With Healed Infarction: Differentiation Between Arrhythmogenic and Nonarrhythmogenic Scar.","authors":"Markus Rottmann, A. Kleber, M. Barkagan, J. Sroubek, E. Leshem, Ayelet Shapira-Daniels, A. Buxton, E. Anter","doi":"10.1161/CIRCEP.119.007879","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007879","url":null,"abstract":"BACKGROUND\u0000In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit.\u0000\u0000\u0000METHODS\u0000In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit.\u0000\u0000\u0000RESULTS\u0000Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT.\u0000\u0000\u0000CONCLUSIONS\u0000Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80764860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.118.007281
Kazuki Iso, Y. Okumura, I. Watanabe, Koichi Nagashima, Keiko Takahashi, M. Arai, Ryuta Watanabe, Yuji Wakamatsu, Naoto Otsuka, S. Yagyu, Sayaka Kurokawa, T. Nakai, Kimie Ohkubo, A. Hirayama
BACKGROUND Ganglionated plexi (GPs) play an important role in both the initiation and maintenance of atrial fibrillation (AF). GPs can be located by using continuous high-frequency stimulation (HFS) to elicit a vagal response, but whether the vagal response phenomenon is common to patients without AF is unknown. METHODS HFS of the left atrial GPs was performed in 42 patients (aged 58.0±10.2 years) undergoing ablation for AF and 21 patients (aged 53.2±12.8 years) undergoing ablation for a left-sided accessory pathway. The HFS (20 Hz, 25 mA, 10-ms pulse duration) was applied for 5 seconds at 3 sites within the presumed anatomic area of each of the 5 major left atrial GPs (for a total of 15 sites per patient). We defined vagal response to HFS as prolongation of the R-R interval by >50% in comparison to the mean pre-HFS R-R interval averaged over 10 beats and active-GP areas as areas in which a vagal response was elicited. RESULTS Overall, more active-GP areas were found in the AF group patients than in the non-AF group patients, and at all 5 major GPs, the maximum R-R interval during HFS was significantly prolonged in the AF patients. After multivariate adjustment, association was established between the total number of vagal response sites and the presence of AF. Conclusions The significant increase in vagal responses elicited in patients with AF compared with responses in non-AF patients suggests that vagal responses to HFS reflect abnormally increased GP activity specific to AF substrates.
{"title":"Is Vagal Response During Left Atrial Ganglionated Plexi Stimulation a Normal Phenomenon?: Comparison Between Patients With and Without Atrial Fibrillation.","authors":"Kazuki Iso, Y. Okumura, I. Watanabe, Koichi Nagashima, Keiko Takahashi, M. Arai, Ryuta Watanabe, Yuji Wakamatsu, Naoto Otsuka, S. Yagyu, Sayaka Kurokawa, T. Nakai, Kimie Ohkubo, A. Hirayama","doi":"10.1161/CIRCEP.118.007281","DOIUrl":"https://doi.org/10.1161/CIRCEP.118.007281","url":null,"abstract":"BACKGROUND\u0000Ganglionated plexi (GPs) play an important role in both the initiation and maintenance of atrial fibrillation (AF). GPs can be located by using continuous high-frequency stimulation (HFS) to elicit a vagal response, but whether the vagal response phenomenon is common to patients without AF is unknown.\u0000\u0000\u0000METHODS\u0000HFS of the left atrial GPs was performed in 42 patients (aged 58.0±10.2 years) undergoing ablation for AF and 21 patients (aged 53.2±12.8 years) undergoing ablation for a left-sided accessory pathway. The HFS (20 Hz, 25 mA, 10-ms pulse duration) was applied for 5 seconds at 3 sites within the presumed anatomic area of each of the 5 major left atrial GPs (for a total of 15 sites per patient). We defined vagal response to HFS as prolongation of the R-R interval by >50% in comparison to the mean pre-HFS R-R interval averaged over 10 beats and active-GP areas as areas in which a vagal response was elicited.\u0000\u0000\u0000RESULTS\u0000Overall, more active-GP areas were found in the AF group patients than in the non-AF group patients, and at all 5 major GPs, the maximum R-R interval during HFS was significantly prolonged in the AF patients. After multivariate adjustment, association was established between the total number of vagal response sites and the presence of AF. Conclusions The significant increase in vagal responses elicited in patients with AF compared with responses in non-AF patients suggests that vagal responses to HFS reflect abnormally increased GP activity specific to AF substrates.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79671695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007519
Wassim Mosleh, Sharma Kattel, Hardik Bhatt, Zaid Al-Jebaje, Sahoor Khan, Tanvi Shah, Suraj Dahal, Charl Khalil, Kevin Frodey, John Elibol, Swati D Sonkawade, Husam Ghanim, Brian Page, Milind R Chaudhari, Umesh C Sharma
{"title":"Galectin-3 as a Risk Predictor of Mortality in Survivors of Out-of-Hospital Cardiac Arrest.","authors":"Wassim Mosleh, Sharma Kattel, Hardik Bhatt, Zaid Al-Jebaje, Sahoor Khan, Tanvi Shah, Suraj Dahal, Charl Khalil, Kevin Frodey, John Elibol, Swati D Sonkawade, Husam Ghanim, Brian Page, Milind R Chaudhari, Umesh C Sharma","doi":"10.1161/CIRCEP.119.007519","DOIUrl":"10.1161/CIRCEP.119.007519","url":null,"abstract":"","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6777856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86608981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007545
V. Essebag, J. Healey, J. Joza, P. Nery, E. Kalfon, T. Leiria, A. Verma, F. Ayala-Paredes, B. Coutu, G. Sumner, G. Becker, F. Philippon, J. Eikelboom, R. Sandhu, John Sapp, R. Leather, D. Yung, B. Thibault, C. Simpson, K. Ahmad, Satish C. Toal, M. Sturmer, K. Kavanagh, E. Crystal, G. Wells, A. Krahn, D. Birnie
BACKGROUND Oral anticoagulant use is common among patients undergoing pacemaker or defibrillator surgery. BRUISE CONTROL (Bridge or Continue Coumadin for Device Surgery Randomized Controlled Trial; NCT00800137) demonstrated that perioperative warfarin continuation reduced clinically significant hematomas (CSH) by 80% compared with heparin bridging (3.5% versus 16%). BRUISE-CONTROL-2 (NCT01675076) observed a similarly low risk of CSH when comparing continued versus interrupted direct oral anticoagulant (2.1% in both groups). Using patient level data from both trials, the current study aims to: (1) evaluate the effect of concomitant antiplatelet therapy on CSH, and (2) understand the relative risk of CSH in patients treated with direct oral anticoagulant versus continued warfarin. METHODS We analyzed 1343 patients included in BRUISE-CONTROL-1 and BRUISE-CONTROL-2. The primary outcome for both trials was CSH. There were 408 patients identified as having continued either a single or dual antiplatelet agent at the time of device surgery. RESULTS Antiplatelet use (versus nonuse) was associated with CSH in 9.8% versus 4.3% of patients (P<0.001), and remained a strong independent predictor after multivariable adjustment (odds ratio, 1.965; 95% CI, 1.202-3.213; P=0.0071). In multivariable analysis, adjusting for antiplatelet use, there was no significant difference in CSH observed between direct oral anticoagulant use compared with continued warfarin (odds ratio, 0.858; 95% CI, 0.375-1.963; P=0.717). CONCLUSIONS Concomitant antiplatelet therapy doubled the risk of CSH during device surgery. No difference in CSH was found between direct oral anticoagulant versus continued warfarin. In anticoagulated patients undergoing elective or semi-urgent device surgery, the patient specific benefit/risk of holding an antiplatelet should be carefully considered. CLINICAL TRIAL REGISTRATION URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00800137, NCT01675076.
{"title":"Effect of Direct Oral Anticoagulants, Warfarin, and Antiplatelet Agents on Risk of Device Pocket Hematoma: Combined Analysis of BRUISE CONTROL 1 and 2.","authors":"V. Essebag, J. Healey, J. Joza, P. Nery, E. Kalfon, T. Leiria, A. Verma, F. Ayala-Paredes, B. Coutu, G. Sumner, G. Becker, F. Philippon, J. Eikelboom, R. Sandhu, John Sapp, R. Leather, D. Yung, B. Thibault, C. Simpson, K. Ahmad, Satish C. Toal, M. Sturmer, K. Kavanagh, E. Crystal, G. Wells, A. Krahn, D. Birnie","doi":"10.1161/CIRCEP.119.007545","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007545","url":null,"abstract":"BACKGROUND\u0000Oral anticoagulant use is common among patients undergoing pacemaker or defibrillator surgery. BRUISE CONTROL (Bridge or Continue Coumadin for Device Surgery Randomized Controlled Trial; NCT00800137) demonstrated that perioperative warfarin continuation reduced clinically significant hematomas (CSH) by 80% compared with heparin bridging (3.5% versus 16%). BRUISE-CONTROL-2 (NCT01675076) observed a similarly low risk of CSH when comparing continued versus interrupted direct oral anticoagulant (2.1% in both groups). Using patient level data from both trials, the current study aims to: (1) evaluate the effect of concomitant antiplatelet therapy on CSH, and (2) understand the relative risk of CSH in patients treated with direct oral anticoagulant versus continued warfarin.\u0000\u0000\u0000METHODS\u0000We analyzed 1343 patients included in BRUISE-CONTROL-1 and BRUISE-CONTROL-2. The primary outcome for both trials was CSH. There were 408 patients identified as having continued either a single or dual antiplatelet agent at the time of device surgery.\u0000\u0000\u0000RESULTS\u0000Antiplatelet use (versus nonuse) was associated with CSH in 9.8% versus 4.3% of patients (P<0.001), and remained a strong independent predictor after multivariable adjustment (odds ratio, 1.965; 95% CI, 1.202-3.213; P=0.0071). In multivariable analysis, adjusting for antiplatelet use, there was no significant difference in CSH observed between direct oral anticoagulant use compared with continued warfarin (odds ratio, 0.858; 95% CI, 0.375-1.963; P=0.717).\u0000\u0000\u0000CONCLUSIONS\u0000Concomitant antiplatelet therapy doubled the risk of CSH during device surgery. No difference in CSH was found between direct oral anticoagulant versus continued warfarin. In anticoagulated patients undergoing elective or semi-urgent device surgery, the patient specific benefit/risk of holding an antiplatelet should be carefully considered.\u0000\u0000\u0000CLINICAL TRIAL REGISTRATION\u0000URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00800137, NCT01675076.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81911888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007549
J. Ramírez, S. van Duijvenboden, N. Aung, P. Laguna, E. Pueyo, A. Tinker, P. Lambiase, M. Orini, P. Munroe
BACKGROUND Early prediction of cardiovascular risk in the general population remains an important issue. The T-wave morphology restitution (TMR), an ECG marker quantifying ventricular repolarization dynamics, is strongly associated with cardiovascular mortality in patients with heart failure. Our aim was to evaluate the cardiovascular prognostic value of TMR in a UK middle-aged population and identify any genetic contribution. METHODS We analyzed ECG recordings from 55 222 individuals from a UK middle-aged population undergoing an exercise stress test in UK Biobank (UKB). TMR was used to measure ventricular repolarization dynamics, exposed in this cohort by exercise (TMR during exercise, TMRex) and recovery from exercise (TMR during recovery, TMRrec). The primary end point was cardiovascular events; secondary end points were all-cause mortality, ventricular arrhythmias, and atrial fibrillation with median follow-up of 7 years. Genome-wide association studies for TMRex and TMRrec were performed, and genetic risk scores were derived and tested for association in independent samples from the full UKB cohort (N=360 631). RESULTS A total of 1743 (3.2%) individuals in UKB who underwent the exercise stress test had a cardiovascular event, and TMRrec was significantly associated with cardiovascular events (hazard ratio, 1.11; P=5×10-7), independent of clinical variables and other ECG markers. TMRrec was also associated with all-cause mortality (hazard ratio, 1.10) and ventricular arrhythmias (hazard ratio, 1.16). We identified 12 genetic loci in total for TMRex and TMRrec, of which 9 are associated with another ECG marker. Individuals in the top 20% of the TMRrec genetic risk score were significantly more likely to have a cardiovascular event in the full UKB cohort (18 997, 5.3%) than individuals in the bottom 20% (hazard ratio, 1.07; P=6×10-3). CONCLUSIONS TMR and TMR genetic risk scores are significantly associated with cardiovascular risk in a UK middle-aged population, supporting the hypothesis that increased spatio-temporal heterogeneity of ventricular repolarization is a substrate for cardiovascular risk and the validity of TMR as a cardiovascular risk predictor.
{"title":"Cardiovascular Predictive Value and Genetic Basis of Ventricular Repolarization Dynamics.","authors":"J. Ramírez, S. van Duijvenboden, N. Aung, P. Laguna, E. Pueyo, A. Tinker, P. Lambiase, M. Orini, P. Munroe","doi":"10.1161/CIRCEP.119.007549","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007549","url":null,"abstract":"BACKGROUND\u0000Early prediction of cardiovascular risk in the general population remains an important issue. The T-wave morphology restitution (TMR), an ECG marker quantifying ventricular repolarization dynamics, is strongly associated with cardiovascular mortality in patients with heart failure. Our aim was to evaluate the cardiovascular prognostic value of TMR in a UK middle-aged population and identify any genetic contribution.\u0000\u0000\u0000METHODS\u0000We analyzed ECG recordings from 55 222 individuals from a UK middle-aged population undergoing an exercise stress test in UK Biobank (UKB). TMR was used to measure ventricular repolarization dynamics, exposed in this cohort by exercise (TMR during exercise, TMRex) and recovery from exercise (TMR during recovery, TMRrec). The primary end point was cardiovascular events; secondary end points were all-cause mortality, ventricular arrhythmias, and atrial fibrillation with median follow-up of 7 years. Genome-wide association studies for TMRex and TMRrec were performed, and genetic risk scores were derived and tested for association in independent samples from the full UKB cohort (N=360 631).\u0000\u0000\u0000RESULTS\u0000A total of 1743 (3.2%) individuals in UKB who underwent the exercise stress test had a cardiovascular event, and TMRrec was significantly associated with cardiovascular events (hazard ratio, 1.11; P=5×10-7), independent of clinical variables and other ECG markers. TMRrec was also associated with all-cause mortality (hazard ratio, 1.10) and ventricular arrhythmias (hazard ratio, 1.16). We identified 12 genetic loci in total for TMRex and TMRrec, of which 9 are associated with another ECG marker. Individuals in the top 20% of the TMRrec genetic risk score were significantly more likely to have a cardiovascular event in the full UKB cohort (18 997, 5.3%) than individuals in the bottom 20% (hazard ratio, 1.07; P=6×10-3).\u0000\u0000\u0000CONCLUSIONS\u0000TMR and TMR genetic risk scores are significantly associated with cardiovascular risk in a UK middle-aged population, supporting the hypothesis that increased spatio-temporal heterogeneity of ventricular repolarization is a substrate for cardiovascular risk and the validity of TMR as a cardiovascular risk predictor.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86524428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007822
Alireza Sepehri Shamloo, N. Dagres, G. Hindricks
October 2019 1 Alireza Sepehri Shamloo, MD Nikolaos Dagres, MD Gerhard Hindricks, MD To the Editor: The term cognitive function in the context of cardiac arrhythmias was first introduced 30 years ago when evidence of cognitive impairment was reported in patients with chronic atrial fibrillation (AF). During the last decades, the topic of cognitive function assessment in AF patients has emerged as a hot topic in the field of electrophysiology; >50 studies have investigated the relationship between these 2 significant public health concerns so far.1 The recently published study conducted by Jin et al2 is groundbreaking and not only confirms findings previously reported by Bunch et al3 about the positive impact of AF ablation on cognitive function but also emphasizes the importance of considering patient-centered outcomes as end points in clinical trials. During the last few decades, hundreds of studies in the field of cardiac arrhythmias have investigated the impact of different therapeutic strategies on major clinical variables including bleeding, stroke, arrhythmia recurrence, and mortality; and a number of them have covered the psychocognitive status as main outcomes. We think that the findings of this current study call to attention the importance of including patient-centered outcomes and also patient-reported outcomes as end points in clinical trials. Currently, management of cognitive dysfunction and controlling the global burden of dementia is one of the top public health priorities designated by the World Health Organization. Moreover, we should not forget that the adherence of treatment and medication intake might be adversely affected by cognitive dysfunction, thereby negatively influencing outcomes and therapy efficiency in the patients suffering from arrhythmias. Although more investigations are required to better define the impact of AF ablation on cognitive status, the recent findings of Jin et al, in conjunction with other studies might be an indication that ablation can improve depression and cognitive function.3–5 This, if supported by further studies, might ultimately lead to the question whether it is time to consider psychocognitive impairments as new indications for AF catheter ablation. Although the current study by Jin et al helps us complete the puzzle of the association between AF, the most common cardiac arrhythmia, and cognitive function, the question which arrhythmia is associated with a greater impairment of cognitive function is still unanswered. Moreover, there is a still a lack of evidence about the impact of different arrhythmia-related procedures, including medical treatment, cardiac device implantation, ablation, or others on patients’ cognitive function. So, when we face this question: Do we need further studies in this field?; the answer is definitely yes. More specifically, the 2 main topics that in our opinion need to be addressed more intensively are (1) the epidemiological understanding of the association b
{"title":"Letter by Sepehri Shamloo et al Regarding Article, \"Atrial Fibrillation Catheter Ablation Improves 1-Year Follow-Up Cognitive Function, Especially in Patients with Impaired Cognitive Function\".","authors":"Alireza Sepehri Shamloo, N. Dagres, G. Hindricks","doi":"10.1161/CIRCEP.119.007822","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007822","url":null,"abstract":"October 2019 1 Alireza Sepehri Shamloo, MD Nikolaos Dagres, MD Gerhard Hindricks, MD To the Editor: The term cognitive function in the context of cardiac arrhythmias was first introduced 30 years ago when evidence of cognitive impairment was reported in patients with chronic atrial fibrillation (AF). During the last decades, the topic of cognitive function assessment in AF patients has emerged as a hot topic in the field of electrophysiology; >50 studies have investigated the relationship between these 2 significant public health concerns so far.1 The recently published study conducted by Jin et al2 is groundbreaking and not only confirms findings previously reported by Bunch et al3 about the positive impact of AF ablation on cognitive function but also emphasizes the importance of considering patient-centered outcomes as end points in clinical trials. During the last few decades, hundreds of studies in the field of cardiac arrhythmias have investigated the impact of different therapeutic strategies on major clinical variables including bleeding, stroke, arrhythmia recurrence, and mortality; and a number of them have covered the psychocognitive status as main outcomes. We think that the findings of this current study call to attention the importance of including patient-centered outcomes and also patient-reported outcomes as end points in clinical trials. Currently, management of cognitive dysfunction and controlling the global burden of dementia is one of the top public health priorities designated by the World Health Organization. Moreover, we should not forget that the adherence of treatment and medication intake might be adversely affected by cognitive dysfunction, thereby negatively influencing outcomes and therapy efficiency in the patients suffering from arrhythmias. Although more investigations are required to better define the impact of AF ablation on cognitive status, the recent findings of Jin et al, in conjunction with other studies might be an indication that ablation can improve depression and cognitive function.3–5 This, if supported by further studies, might ultimately lead to the question whether it is time to consider psychocognitive impairments as new indications for AF catheter ablation. Although the current study by Jin et al helps us complete the puzzle of the association between AF, the most common cardiac arrhythmia, and cognitive function, the question which arrhythmia is associated with a greater impairment of cognitive function is still unanswered. Moreover, there is a still a lack of evidence about the impact of different arrhythmia-related procedures, including medical treatment, cardiac device implantation, ablation, or others on patients’ cognitive function. So, when we face this question: Do we need further studies in this field?; the answer is definitely yes. More specifically, the 2 main topics that in our opinion need to be addressed more intensively are (1) the epidemiological understanding of the association b","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73241187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007863
C. DeSimone, D. DeSimone, Y. Cha
The use of oral anticoagulation and antiplatelet therapy is common among patients undergoing placement of pacemakers or defibrillators. This comes as no surprise as patients requiring cardiac implantable electronic devices (CIEDs) are older and more often have comorbidities such as atrial fibrillation, ischemic cardiomyopathy, or both. Continuation of anticoagulation confers stroke prophylaxis, whereas antiplatelet continuation is necessary in those with recent stent placement. In patients with high stroke risk, heparin bridging can be used in the perioperative setting. The concern that comes to fruition at the time of CIED implantation is the risk of not achieving adequate hemostasis intraprocedurally, as well as the risk of postimplant device pocket hematoma (DPH). DPH is fraught with several issues including patient comorbidities such as pain/discomfort, need for pocket reintervention for hematoma evacuation, increased infection risk, and significant costs associated with length of hospitalization and additional procedures.1–3
{"title":"Contemporary Management of Antiplatelet and Anticoagulation for Cardiac Implantable Device Procedures.","authors":"C. DeSimone, D. DeSimone, Y. Cha","doi":"10.1161/CIRCEP.119.007863","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007863","url":null,"abstract":"The use of oral anticoagulation and antiplatelet therapy is common among patients undergoing placement of pacemakers or defibrillators. This comes as no surprise as patients requiring cardiac implantable electronic devices (CIEDs) are older and more often have comorbidities such as atrial fibrillation, ischemic cardiomyopathy, or both. Continuation of anticoagulation confers stroke prophylaxis, whereas antiplatelet continuation is necessary in those with recent stent placement. In patients with high stroke risk, heparin bridging can be used in the perioperative setting. The concern that comes to fruition at the time of CIED implantation is the risk of not achieving adequate hemostasis intraprocedurally, as well as the risk of postimplant device pocket hematoma (DPH). DPH is fraught with several issues including patient comorbidities such as pain/discomfort, need for pocket reintervention for hematoma evacuation, increased infection risk, and significant costs associated with length of hospitalization and additional procedures.1–3","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72645750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.117.005557
R. Ramirez, Y. Takemoto, R. Martins, D. Filgueiras-Rama, S. Ennis, S. Mironov, Sandesh Bhushal, M. Deo, S. Rajamani, O. Berenfeld, L. Belardinelli, J. Jalife, S. Pandit
BACKGROUND Ranolazine inhibits Na+ current (INa), but whether it can convert atrial fibrillation (AF) to sinus rhythm remains unclear. We investigated antiarrhythmic mechanisms of ranolazine in sheep models of paroxysmal (PxAF) and persistent AF (PsAF). METHODS PxAF was maintained during acute stretch (N=8), and PsAF was induced by long-term atrial tachypacing (N=9). Isolated, Langendorff-perfused sheep hearts were optically mapped. RESULTS In PxAF ranolazine (10 μmol/L) reduced dominant frequency from 8.3±0.4 to 6.2±0.5 Hz (P<0.01) before converting to sinus rhythm, decreased singularity point density from 0.070±0.007 to 0.039±0.005 cm-2 s-1 (P<0.001) in left atrial epicardium (LAepi), and prolonged AF cycle length (AFCL); rotor duration, tip trajectory, and variance of AFCL were unaltered. In PsAF, ranolazine reduced dominant frequency (8.3±0.5 to 6.5±0.4 Hz; P<0.01), prolonged AFCL, increased the variance of AFCL, had no effect on singularity point density (0.048±0.011 to 0.042±0.016 cm-2 s-1; P=ns) and failed to convert AF to sinus rhythm. Doubling the ranolazine concentration (20 μmol/L) or supplementing with dofetilide (1 μmol/L) failed to convert PsAF to sinus rhythm. In computer simulations of rotors, reducing INa decreased dominant frequency, increased tip meandering and produced vortex shedding on wave interaction with unexcitable regions. CONCLUSIONS PxAF and PsAF respond differently to ranolazine. Cardioversion in the former can be attributed partly to decreased dominant frequency and singularity point density, and prolongation of AFCL. In the latter, increased dispersion of AFCL and likely vortex shedding contributes to rotor formation, compensating for any rotor loss, and may underlie the inefficacy of ranolazine to terminate PsAF.
{"title":"Mechanisms by Which Ranolazine Terminates Paroxysmal but Not Persistent Atrial Fibrillation.","authors":"R. Ramirez, Y. Takemoto, R. Martins, D. Filgueiras-Rama, S. Ennis, S. Mironov, Sandesh Bhushal, M. Deo, S. Rajamani, O. Berenfeld, L. Belardinelli, J. Jalife, S. Pandit","doi":"10.1161/CIRCEP.117.005557","DOIUrl":"https://doi.org/10.1161/CIRCEP.117.005557","url":null,"abstract":"BACKGROUND\u0000Ranolazine inhibits Na+ current (INa), but whether it can convert atrial fibrillation (AF) to sinus rhythm remains unclear. We investigated antiarrhythmic mechanisms of ranolazine in sheep models of paroxysmal (PxAF) and persistent AF (PsAF).\u0000\u0000\u0000METHODS\u0000PxAF was maintained during acute stretch (N=8), and PsAF was induced by long-term atrial tachypacing (N=9). Isolated, Langendorff-perfused sheep hearts were optically mapped.\u0000\u0000\u0000RESULTS\u0000In PxAF ranolazine (10 μmol/L) reduced dominant frequency from 8.3±0.4 to 6.2±0.5 Hz (P<0.01) before converting to sinus rhythm, decreased singularity point density from 0.070±0.007 to 0.039±0.005 cm-2 s-1 (P<0.001) in left atrial epicardium (LAepi), and prolonged AF cycle length (AFCL); rotor duration, tip trajectory, and variance of AFCL were unaltered. In PsAF, ranolazine reduced dominant frequency (8.3±0.5 to 6.5±0.4 Hz; P<0.01), prolonged AFCL, increased the variance of AFCL, had no effect on singularity point density (0.048±0.011 to 0.042±0.016 cm-2 s-1; P=ns) and failed to convert AF to sinus rhythm. Doubling the ranolazine concentration (20 μmol/L) or supplementing with dofetilide (1 μmol/L) failed to convert PsAF to sinus rhythm. In computer simulations of rotors, reducing INa decreased dominant frequency, increased tip meandering and produced vortex shedding on wave interaction with unexcitable regions.\u0000\u0000\u0000CONCLUSIONS\u0000PxAF and PsAF respond differently to ranolazine. Cardioversion in the former can be attributed partly to decreased dominant frequency and singularity point density, and prolongation of AFCL. In the latter, increased dispersion of AFCL and likely vortex shedding contributes to rotor formation, compensating for any rotor loss, and may underlie the inefficacy of ranolazine to terminate PsAF.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87007134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007880
M. Jin, Tae‐Hoon Kim, Ki-Woon Kang, H. Yu, J. Uhm, B. Joung, Moon‐Hyoung Lee, Eosu Kim, H. Pak
{"title":"Response by Jin et al to Letter Regarding Article, \"Atrial Fibrillation Catheter Ablation Improves 1-Year Follow-Up Cognitive Function, Especially in Patients With Impaired Cognitive Function\".","authors":"M. Jin, Tae‐Hoon Kim, Ki-Woon Kang, H. Yu, J. Uhm, B. Joung, Moon‐Hyoung Lee, Eosu Kim, H. Pak","doi":"10.1161/CIRCEP.119.007880","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007880","url":null,"abstract":"","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83674885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-01DOI: 10.1161/CIRCEP.119.007598
E. Donnellan, O. Wazni, M. Kanj, A. Hussein, B. Baranowski, B. Lindsay, A. Aminian, W. Jaber, P. Schauer, W. Saliba
BACKGROUND Morbid obesity is associated with unacceptable high recurrence rates following atrial fibrillation ablation. The role of risk-factor modification including weight loss and improved glycemic control in reducing arrhythmia recurrence following ablation has been highlighted in recent years. In this study, we compared arrhythmia recurrence rates in morbidly obese patients who underwent prior bariatric surgery (BS) with those of nonobese patients following atrial fibrillation ablation in addition to morbidly obese patients who did not undergo BS. METHODS This was a single-center observational cohort study. We matched 51 morbidly obese patients [body mass index ≥40 kg/m2] who had undergone prior BS in a 2:1 manner with 102 nonobese patients and 102 morbidly obese patients without prior BS on the basis of age, sex, and timing of atrial fibrillation ablation. Our primary outcome of interest was arrhythmia recurrence. RESULTS From the time of BS to ablation, BS was associated with a significant reduction in body mass index (47.6±9.3 to 36.7±7; P<0.0001), glycated hemoglobin (6.7±1.5 to 5.8±0.6; P<0.0001), and systolic blood pressure (145±13 to 118±11; P<0.0001). During a mean follow-up of 29±13 months following ablation, recurrent arrhythmia occurred in 10/51 (20%) patients in the BS group compared with 25/102 (24.5%) patients in the nonobese group and 56 (55%) patients in the non-BS morbidly obese group (P<0.0001). No procedural complications were observed in the BS group. CONCLUSIONS Bariatric surgery is associated with a reduction in arrhythmia recurrence following atrial fibrillation ablation in morbidly obese patients to those of nonobese patients. Morbidly obese patients should be considered for BS before atrial fibrillation ablation.
{"title":"Outcomes of Atrial Fibrillation Ablation in Morbidly Obese Patients Following Bariatric Surgery Compared With a Nonobese Cohort.","authors":"E. Donnellan, O. Wazni, M. Kanj, A. Hussein, B. Baranowski, B. Lindsay, A. Aminian, W. Jaber, P. Schauer, W. Saliba","doi":"10.1161/CIRCEP.119.007598","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007598","url":null,"abstract":"BACKGROUND\u0000Morbid obesity is associated with unacceptable high recurrence rates following atrial fibrillation ablation. The role of risk-factor modification including weight loss and improved glycemic control in reducing arrhythmia recurrence following ablation has been highlighted in recent years. In this study, we compared arrhythmia recurrence rates in morbidly obese patients who underwent prior bariatric surgery (BS) with those of nonobese patients following atrial fibrillation ablation in addition to morbidly obese patients who did not undergo BS.\u0000\u0000\u0000METHODS\u0000This was a single-center observational cohort study. We matched 51 morbidly obese patients [body mass index ≥40 kg/m2] who had undergone prior BS in a 2:1 manner with 102 nonobese patients and 102 morbidly obese patients without prior BS on the basis of age, sex, and timing of atrial fibrillation ablation. Our primary outcome of interest was arrhythmia recurrence.\u0000\u0000\u0000RESULTS\u0000From the time of BS to ablation, BS was associated with a significant reduction in body mass index (47.6±9.3 to 36.7±7; P<0.0001), glycated hemoglobin (6.7±1.5 to 5.8±0.6; P<0.0001), and systolic blood pressure (145±13 to 118±11; P<0.0001). During a mean follow-up of 29±13 months following ablation, recurrent arrhythmia occurred in 10/51 (20%) patients in the BS group compared with 25/102 (24.5%) patients in the nonobese group and 56 (55%) patients in the non-BS morbidly obese group (P<0.0001). No procedural complications were observed in the BS group.\u0000\u0000\u0000CONCLUSIONS\u0000Bariatric surgery is associated with a reduction in arrhythmia recurrence following atrial fibrillation ablation in morbidly obese patients to those of nonobese patients. Morbidly obese patients should be considered for BS before atrial fibrillation ablation.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83184112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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